Neuronal cells are extremely vulnerable and have a limited capacity for self-repair in response to injury. For those reasons, there is obvious interest in limiting neuronal damage. Mechanisms and strategies used in order to protect against neuronal injury, apoptosis, dysfunction, and degeneration in the central nervous system are recognized as neuroprotection. Neuroprotection could be achieved through several classes of natural and synthetic neuroprotective agents. However, considering the side effects of synthetic neuroprotective agents, the search for natural neuroprotective agents has received great attention. Recently, an increasing number of studies have identified neuroprotective properties of chitosan and its derivatives; however, there are some significant challenges that must be overcome for the success of this approach. Hence, the objective of this review is to discuss neuroprotective properties of chitosan and its derivatives.
Oxidative stress is a major mediator of cellular injury following ischaemic stroke and reactive oxygen species, like superoxide, have multiple deleterious effects on the components of the neurovascular unit. It is well established that NADPH oxidase is the principal source of superoxide in acute ischaemic stroke and is therefore a target for potential neuroprotective strategies (Moskowitz et al, 2010). Consequently, the second aim of this thesis was to evaluate the potential neuroprotective effect of NADPH oxidase inhibition with low and high dose apocynin following permanent or transient ischaemia. Rats were administered apocynin at a dose of 5mg/kg or 30mg/kg or vehicle, at 5 minutes post-MCAO. Apocynin treatment had no significant effect on infarct volume or functional outcome at 24 hours following permanent MCAO in WKY rats. However, both low and high dose apocynin treatment significantly reduced infarct volume at 72 hours post-MCAO by 60% following 1 hour of ischaemia in Sprague-Dawley ...
TY - JOUR. T1 - Combination therapy for ischemic stroke. T2 - Potential of neuroprotectants plus thrombolytics. AU - Chen, Shang Der. AU - Lee, Jin Moo. AU - Yang, Ding I.. AU - Nassief, Abdullah. AU - Hsu, Chung Y.. PY - 2002. Y1 - 2002. N2 - Thrombolysis improves clinical outcome in patients with acute ischemic stroke. However, only a small fraction of patients receive thrombolytic therapy due to the narrow therapeutic time window available for the treatment in patients with ischemic stroke. A better understanding of the mechanisms underlying ischemic injury may lead to the development of novel therapeutic strategies to reduce brain damage after stroke. Cerebral ischemia triggers a number of pathophysiological and biochemical changes in the brain that present potential targets for therapeutic intervention. Candidate pathways include those regulating cellular calcium influx, excitatory neurotransmitter uptake, and generation of reactive oxygen species, as well as activation of enzymes including ...
Extensive evidence exists that neurodegeneration begins many years before HD can be diagnosed clinically. Therefore, it is most desirable to begin a neuroprotective therapy before or during this premanifest period with the aim of delaying onset, as well as slowing functional decline. Cellular energy depletion is present early in HD and can be ameliorated by creatine, which helps regenerate cellular ATP. Preclinical evidence for creatines potential neuroprotective effects in animal models of HD has been well-documented. Before the clinical efficacy of creatine can be tested in premanifest HD, its long-term safety and tolerability must be assessed in these individuals and its ability to favorably modify biomarkers of HD should also be confirmed. This extension trial will continue to follow eligible individuals who completed the Pre-CREST-X extension study on open-label creatine (up to 30 grams daily) for long term safety and tolerability for an additional 24 months. Other biological and imaging ...
Cannabinoids have been found to have antioxidant properties, unrelated to NMDA receptor antagonism. This new found property makes cannabinoids useful in the treatment and prophylaxis of wide variety of oxidation associated diseases, such as ischemic, age-related, inflammatory and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimers disease, Parkinsons disease and HIV dementia. Nonpsychoactive cannabinoids, such as cannabidoil, are particularly advantageous to use because they avoid toxicity that is encountered with psychoactive cannabinoids at high doses useful in the method of the present invention. A particular disclosed class of cannabinoids useful as neuroprotective antioxidants is formula (I) wherein the R group is independently selected from the group consisting of H, ...
PMID: 31545255 Open Access Sabogal-Guaqueta AM, Hobbie F, Keerthi A, Oun A, Kortholt A, Boddeke E, Dolga A (2019) Biomed Pharmacother Abstract: Mitochondrial dysfunction and inflammation contribute to the initiation and development of several brain pathological conditions, including Alzheimers disease and cerebral ischemia. Linalool is an aromatic plant-derived monoterpene alcohol with reported anti-inflammatory, and anti-oxidant properties. We investigated the role of linalool on glutamate-induced mitochondrial oxidative stress in immortalized neuronal HT-22 cells. Glutamate induced oxidative stress in neuronal cells, as detected by real-time cell impedance measurements, MTT assay, and analysis of Annexin V/PI. Administration of linalool 100 μM reduced cell death mediated by glutamate. Staining of glutamate-stimulated mitochondria by MitoTracker revealed improved morphology in the presence of linalool. Furthermore, we demonstrated a potential neuroprotective effect of linalool in conditions ...
MN-166 Slows Disability Progression Significant Neuroprotective Effects Observed by MRI MediciNova, Inc., a biopharmaceutical company that is publicly traded on
Stroke is an acute brain health issue which causes neuronal damage which has currently no safe and effective neuroprotective treatment approaches. Immediately following a stroke, the brain tissue loses blood perfusion and the center of the infarct deteriorates quickly. This then causes milder ischemia and many brain cells or neurons will result in delayed death which can take up to several hours or even days. Research studies show that the mechanism of cell death is mainly NMDA receptor-dependent excitotoxicity. In ischemic areas, extracellular glutamate levels increase while preventing glutamate release, synaptic activity, or NMDAR activation which was capable of limiting cell death in a variety of stroke models. Thus, preventing excitotoxicity is an important treatment approach for reducing brain damage and improving patient outcome measures following a stroke, and this has definitely encouraged extensive efforts towards developing NMDA receptor-based stroke treatment approaches over the last ...
Methods PCR, Western Blotting and Immunohistochemistry was performed according to standard protocols. Brain hemispheres of untreated Wistar rats (p1-p15) were evaluated under developmental aspects of TSG-6. LPS-treated rats (0.25mg/kg LPS i.p. on p3) were evaluated under pathological aspects of TSG-6. To evaluate whether exogenous rhTSG-6 reduces inflammatory-induced brain injury, newborn Wistar rats, exposed to LPS at p3, were treated with rhTSG-6 i.p. (four repetitive doses of 2.25mg/kg every 12h, first dose three hours before LPS-injection).. ...
Cannabinoids have been found to have antioxidant properties, unrelated to NMDA receptor antagonism. This new found property makes cannabinoids useful in the treatment and prophylaxis of wide variety of oxidation associated diseases, such as ischemic, age-related, inflammatory and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimers disease, Parkinsons disease and HIV dementia. Nonpsychoactive cannabinoids, such as cannabidoil, are particularly advantageous to use because they avoid toxicity that is encountered with psychoactive cannabinoids at high doses useful in the method of the present invention.
Retinal ischemia can be effectively modeled by permanent bilateral common carotid artery occlusion, which leads to chronic hypoperfusion-induced degeneration in the entire rat retina. The complex pathways leading to retinal cell death offer a complex approach of neuroprotective strategies. In the present review we summarize recent findings with different neuroprotective candidate molecules. We describe the protective effects of intravitreal treatment with: (i) urocortin 2; (ii) a mitochondrial ATP-sensitive K+ channel opener, diazoxide; (iii) a neurotrophic factor, pituitary adenylate cyclase activating polypeptide; and (iv) a novel poly(ADP-ribose) polymerase inhibitor (HO3089). The retinoprotective effects are demonstrated with morphological description and effects on apoptotic pathways using molecular biological techniques.
TY - JOUR. T1 - GOSPEL. T2 - a neuroprotective protein that binds to GAPDH upon S-nitrosylation.. AU - Sen, Nilkantha. AU - Hara, Makoto R.. AU - Ahmad, Abdullah Shafique. AU - Cascio, Matthew B.. AU - Kamiya, Atsushi. AU - Ehmsen, Jeffrey T.. AU - Aggrawal, Nishant. AU - Hester, Lynda. AU - Doré, Sylvain. AU - Snyder, Solomon H.. AU - Sawa, Akira. PY - 2009/7/16. Y1 - 2009/7/16. N2 - We recently reported a cell death cascade whereby cellular stressors activate nitric oxide formation leading to S-nitrosylation of GAPDH that binds to Siah and translocates to the nucleus. The nuclear GAPDH/Siah complex augments p300/CBP-associated acetylation of nuclear proteins, including p53, which mediate cell death. We report a 52 kDa cytosolic protein, GOSPEL, which physiologically binds GAPDH, in competition with Siah, retaining GAPDH in the cytosol and preventing its nuclear translocation. GOSPEL is neuroprotective, as its overexpression prevents NMDA-glutamate excitotoxicity while its depletion enhances ...
TY - JOUR. T1 - Ghrelin-AMPK signaling mediates the neuroprotective effects of calorie restriction in Parkinsons Disease. AU - Bayliss, Jacqueline A.. AU - Lemus, Moyra B.. AU - Stark, Romana. AU - Santos, Vanessa V. AU - Thompson, Aiysha. AU - Rees, Daniel J.. AU - Galic, Sandra. AU - Elsworth, John D.. AU - Kemp, Bruce E.. AU - Davies, Jeffrey S.. AU - Andrews, Zane B.. PY - 2016/3/9. Y1 - 2016/3/9. N2 - Calorie restriction (CR) is neuroprotective in Parkinsons disease (PD) although the mechanisms are unknown. In this study we hypothesized that elevated ghrelin, a gut hormone with neuroprotective properties, during CR prevents neurodegeneration in an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD. CR attenuated the MPTP-induced loss of substantia nigra (SN) dopamine neurons and striatal dopamine turnover in ghrelin WT but not KO mice, demonstrating that ghrelin mediates CRs neuroprotective effect. CR elevated phosphorylated AMPK and ACC levels in the striatum of WT but not ...
TY - JOUR. T1 - Quantitative evaluation of the neuroprotective effects of a short-acting β-adrenoceptor antagonist at a clinical dose on forebrain ischemia in gerbils. T2 - Effects of esmolol on ischemic depolarization and histologic outcome of hippocampal CA1. AU - Danura, Tetsuya. AU - Takeda, Yoshimasa. AU - Shiraishi, Kensuke. AU - Naito, Hiromichi. AU - Mizoue, Ryoichi. AU - Sato, Sachiko. AU - Morita, Kiyoshi. PY - 2013/7. Y1 - 2013/7. N2 - Background: Neuroprotective effects of esmolol in laboratory and clinical settings have been reported. The present study was designed to quantitatively evaluate the neuroprotective effects of esmolol using logistic regression curves and extracellular potentials. Materials and Methods: In 42 gerbils, bilateral occlusion of common carotid arteries was performed for 3, 5, or 7 minutes (n=7 in each group). In treated animals, esmolol (200 μg/kg/min) was administered for 90 minutes, 30 minutes before the onset of ischemia. Direct current potentials were ...
OBJECTIVE: To assess platelet activating factor (PAF) antagonists, potent neuroprotective agents in experimental cerebral dysfunction, in clinical practice. DESIGN: Double blind, minimised, placebo controlled trial of low and high dose PAF antagonist (lexipafant). SETTING: Cardiac surgery unit. PATIENTS: 150 patients undergoing coronary artery bypass graft (CABG) surgery using cardiopulmonary bypass. INTERVENTIONS: Randomisation to placebo, low dose (10 mg) or high dose (100 mg) lexipafant. MAIN OUTCOME MEASURES: Incidence of impairment on four established cognitive tests, undertaken before, five days, and three months after CABG, examined by three methods for defining impairment. RESULTS: The three groups were similar with respect to preoperative and intraoperative factors. Observed levels of cognitive impairment were less than had been predicted from previous studies. There was no difference in the groups in cognitive change scores at five days or three months. Group mean analysis showed significant
Previous studies have demonstrated that aripiprazole (APZ), a third‑generation atypical antipsychotic drug, exhibits anti‑depressant and neuroprotective effects by promoting dopaminergic neuronal cell recovery in stroke. To investigate the neuroprotective effects of APZ, behavioral and histopathological experiments were performed in the current study a mouse model of middle cerebral artery occlusion (MCAO)‑induced ischemia following administration of APZ. The subacute phase of ischemic assaults was divided into 3 periods, each with a duration of 5 days, according to the start of APZ (3 mg/kg) administration (1‑5, 5‑9 or 10‑14 days following MCAO). The beneficial effects of APZ on motor behavior demonstrated in the cylinder, rotarod and wire suspension tests were greatest when APZ was administered 1‑5 days following MCAO, with clear improvements in motor function compared with vehicle‑treated mice. Histopathological analysis revealed that prominent atrophic changes occurred in the ...
Provided are methods for treatment and prevention of ischemia- reperfusion injury and chronic intermittent hypoxia related injury through administering a neuroprotective compound. A subject benefiting from the method of the invention may be prescribed or undergoing anti-VEGF treatment, for example an IV AV treatment regimen, or may be diagnosed with a disorder such as sleep apnea.
Cochran, Kelly, Neuroprotective drug treatment in DBA/2J glaucoma. (2015). Summer and Academic Year Student Reports. 2493 ...
Abstract: : Purpose: Ca2+ overload has been implicated in neurodegeneration, and Ca2+ channel blockers have been proposed as potential neuroprotective agents in prevention of retinal ganglion cell death in glaucoma. We have investigated the role of the L-type voltage-operated Ca2+ channel in shaping Ca2+ signalling events in cultured human retinal neurons. Methods: Human retinas were obtained from donor eyes within 24 hours post mortem. The neural retina was dissected from the globe and dissociated using papain. Cells were plated onto glass coverslips and maintained in Ham/F12 medium with 10% FCS and 10ng/ml bFGF. Following 1 week in culture, neuronal cells were distinguishable by morphological characteristics. Following Fura-2 incorporation (3µM for 45 minutes at 35°C), changes in cytosolic Ca2+ concentration were monitored in retinal neurons using real-time epifluorescence techniques. Experiments were carried out in the absence of external Mg2+. Glutamate and glutamate agonists were added in ...
Polyphenols or other phytochemicals appear to be potential and promising class of therapeutics for the treatment of diseases with a multifactorial etiology.
Using surrogate biomarkers for disease progression as endpoints in neuroprotective clinical trials may help differentiate symptomatic effects of potential neuroprotective agents from true disease-modifying effects. A systematic review was undertaken to determine what biomarkers for disease progression in Parkinsons disease (PD) exist. MEDLINE and EMBASE (1950-2010) were searched using five search strategies. Abstracts were assessed to identify papers meriting review in full. Studies of participants with idiopathic PD diagnosed by formal criteria or clearly described clinical means were included. We made no restriction on age, disease duration, drug treatment, or study design. We included studies which attempted to draw associations between any tests used to investigate disease progression and any clinical measures of disease progression. The electronic search was validated by hand-searching the two journals from which most included articles came. 183 studies were included: 163 (89%) cross-sectional, 20
On November 17, 2011, in accordance with 35 U.S.C. 209(c)(1) and 37 CFR part 404.7(a)(1)(i), the National Institutes of Health, Department of Health and Human Services, published in the Federal Register, that it is contemplating the grant of an exclusive patent license to practice the invention embodied in U.S. Patent 6,630,507, entitled Cannabinoids as antioxidants and neuroprotectants and PCT Application Serial No. PCT/US99/08769 and foreign equivalents thereof, entitled Cannabinoids as antioxidants and neuroprotectants [HHS Ref. No. E-287-1997/2] to KannaLife Sciences Inc., which has offices in New York, U.S. This patent and its foreign counterparts have been assigned to the Government of the United States of America. The prospective exclusive license territory may be worldwide, and the field of use may be limited to: The development and sale of cannabinoid(s) and cannabidiol(s) based therapeutics as antioxidants and neuroprotectants for use and delivery in humans, for the treatment of ...
Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion.. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4).. In a stroke model rats were made hyperglycemic prior to transient ...
Although enhancing neuronal Ca2+ buffering has neuroprotective potential, we have shown that BAPTA-AM, under select circumstances (moderate insult with NMDA), can also be toxic. This finding reconciles the authors and others previously conflicting conclusions about the utility of Ca2+ buffers as neuroprotectants [Scharfman and Schwartzkroin (1989) vs Abdel-Hamid (1994)] (Baimbridge and Abdel-Hamid, 1992; Dubinsky, 1993; Tymianski et al., 1993c, 1994a). For example, Tymianski et al., working in spinal neurons, suggested that pretreatment with BAPTA-AM was protective against a glutamate challenge when toxicity was assayed within a few hours of the insult. However, Abdel-Hamid and Baimbridge showed in hippocampal neurons that pretreatment with BAPTA-AM before excitotoxin application was toxic at 24 hr (see references above). The disparity of previous findings illustrates the importance of evaluating the time course, the mechanism, and the extent of cell death in excitotoxic paradigms, ...
Authors: Ellwardt E, Zipp F Abstract Multiple sclerosis (MS) is an inflammatory demyelinating autoimmune disorder of the central nervous system (CNS) and one of the leading causes of neurological deficits and disability in young adults in western countries. Current medical treatment mainly influences disease progression via immunomodulatory or immunosuppressive actions. Indeed, MS research has been foremost focused on inflammation in the CNS, but more recent evidence suggests that chronic disability in MS is caused by neurodegeneration. Imaging studies show an early involvement of neurodegeneration as brain atrophy and gray matter lesions can be observed at disease onset. Thus, neuroprotective treatment strategies and the elucidation of the molecular mechanisms underlying neurodege...
Interleukin-6 (IL-6) is a potential neuroprotective factor for retinal ganglion cells (RGCs) exposed to elevated pressure. In glaucomatous retina, IL-6 is prod...
Background and objectives: Neuronal toxicity can be induced by oxidative stress via free radicals production. In recent years, great interest has been expressed to the traditional and herbal medicines. The purpose of this study was to elucidate the neuroprotective activity of Leontice leontopetalum methanol extract against H2O2-stimulated oxidative stress in PC12 cells. Methods: The plantLeontice leontopetalum was selected based on the ethnobotanical approach, which is used traditionally for the treatment of diseases related to inflammation and pain in Turkmen Sahra, Iran. Cytotoxicity of different concentrations of the methanol extract against PC12 cells was evaluated by MTT assay. Then PC12 cells were exposed to H2O2 in the presence or absence of the extract. In the next step, the total protein concentration was measured via Bradford assay and cyclooxygenase inhibition was determined by a screening assay kit. Nitrite accumulated in culture medium of supernatant was measured by Griess reaction. Results
Gonzalez, P., Peluffo, H., Acarin, L., Villaverde, A., Gonzalez, B. and Castellano, B. (2012), Interleukin-10 overexpression does not synergize with the neuroprotective action of RGD-containing vectors after postnatal brain excitotoxicity but modulates the main inflammatory cell responses. J. Neurosci. Res., 90: 143-159. doi: 10.1002/jnr.22741 ...
J147 is a potent neuroprotective and neurotrophic compound. J147 protects against neurotoxicity in cortical neurons in vitro (EC50 = 25 - 200 nM). J147. J147 reverses cognitive impairment in aged Alzheimers disease mice. J147 is an exciting new compound that is extremely potent, safe in animal studies and orally active. J147 is a potential AD therapeutic due to its ability to provide immediate cognition benefits, and it also has the potential to halt and perhaps reverse disease progression in symptomatic animals as demonstrated in these studies.
Endogenous mechanisms of ischemic preconditioning-tolerance have reviled the brains ability to reprogram (precondition) its response to acute ischemia from tha...
This application aims to investigate whether a mechanism used by a virus to block hepatocyte apoptosis can be translated and optimized to block neuronal cell de...
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Predicated on these findings, an increasing number of clinical practices and research favor the treating SCI through A-MSC transplantation. which in turn causes immediate structural harm, some secondary accidents, including hemorrhage, edema, demyelination, and axonal and neuronal necrosis, get excited about the pathological procedure after SCI [1, 2]. Soon after, a fibrous glial scar tissue shaped by infiltrated inflammatory cells, including microglia, fibroblasts, and reactive astrocytes, limitations axon regeneration over the lesion [3, 4]. Strategies concentrating on these unique systems, aswell as regenerative and neuroprotective therapies, are anticipated to be utilized as remedies for SCI. Neuroprotective therapy functions by restricting secondary harm, while neuroregenerative strategies try to substitute the broken cells, axons, and circuits in the spinal-cord [5]. Although few neuroprotective and regenerative therapies that exert helpful results are obtainable [6] straight, cell ...
The purpose of this study is to evaluate the ability of overexpression of Nmnat1 to slow axonal degeneration in two mouse models of optic neuropathy.
Adenosine A1 agonists have potent neuroprotective properties. However, their therapeutic potential is limited by cardiovascular adverse events. These adverse
Advancing methods for evaluating therapeutic response have fostered a new era in glaucoma neuroprotection in which promising candidates are already being investigated in clinical trials and others are poised to begin phase I testing, said Jeffrey L. Goldberg, MD, PhD.
Progressive HIV-1 infection commonly elicits neurologic impairments despite aggressive antiretroviral regimens, and significant improvements in the quality and duration of life may be balanced with demonstrable cognitive decline (49-54). Such decline is linked, in part, to variable penetration of antiretroviral drugs across the blood-brain barrier, difficulties with drug toxicity and compliance, and viral mutation (50-57).. The complex multifactorial pathogenesis of HAND presents therapeutic opportunities with respect to the development of novel adjunctive therapies. For example, viral infection and immune activation of MPs play an essential role in mediated neuronal damage in disease and can be exploited for therapeutic gain (58-60). Medicines that interfere with neuroinflammation or that protect neurons from damage can be expected to have a positive effect on the pathogenesis of HAND. CEP-1347 is a semisynthetic indolocarbazole that inhibits MLKs by acting as a competitive ATP site inhibitor ...
Numerous studies have confirmed the neuroprotective efficacy of ischemic preconditioning in animal models.14 32 33 However, these studies have typically used young subjects, and it was therefore unknown whether similar levels of protection would be obtained in older animals.. In the present study there was significant histological protection of CA1 neurons across 3 anterior-posterior levels of the hippocampus (88.2%, 83.5%, and 89.4% of sham controls) at 10 days in preconditioned animals. The rostral CA1 region is known to be highly vulnerable to cerebral ischemia.11 12 In this study, the degree of neuronal protection found at this level was similar to that seen in similar studies from our laboratory using young (3-month-old) animals.20 32 Interestingly, there was not as rapid nor as great a decline in CA1 cell numbers in the aged animals with longer survival times. Thirty days after ischemic preconditioning there were ≈53%20 and ≈66.5%32 savings of rostral CA1 in the young animals. This is ...
Background: Cannabis and its extracts are now being explored due to their huge health benefits. Although, the effect they elicit, whether on humans or rodents,
A number of recent discoveries indicate that huperzine A, an active herbal medicine employed for the treatment of Alzheimers disease (AD) in China, can afford neuroprotection on in vitro and in vivo models related to mitochondrial dysfunction. Howev
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There is a critical need for surrogate markers that can be used to predict cognitive impairment and to monitor the effects of antiretroviral, or neuroprotective therapy in HIV-infected individuals.
About 15 years ago, I wrote an article about treating Alzheimers disease that divided treatments into two categories: symptomatic and neuroprotectant. There were real options in the former category. But the neuroprotectant idea was more theoretical - more of a coming attractions approach - citing the studies that were underway to identify treatments that would actually save brain cells, protecting those neurons from further harm, and actually slowing or arresting the disease process. Sadly, despite … Read More. ...
Cerebral ischemia resulting from cardiac arrest and stroke is a leading causes of mortality and morbidity. Can the neuroprotective effects of ischemic preconditioning improve outcomes?
PRPS-1 is a regulative for neuroprotection and cells regenerative proliferation, Danielyan KE, Vardanyan R, Paronyan ZK, Barkhudaryants IM, Chailyan SG, Bisharyan MS
The neuroprotective effects of NS 521 were being investigated in Demmark with NeroSearch. However, development has been discontinued.
Former President Olusegun Obasanjo has revealed the aspect of the Peoples Democratic Partys Chairman, Prince Uche Secondus visit that made his heart leapt for joy when the later visited on Thursday.
The present study was to investigate the neuroprotective efficacy and mechanism of Forsythoside B. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion for 1 h followed by reperfusion for 23 h. Rats received an intravenous bolus injection of Forsythoside B at 15 min after reperfusion. The results showed that Forsythoside B at doses higher than 8 mg/kg produced a significant neuroprotective potential in cerebral ischemia and reperfusion rats. Forsythoside B (20 mg/kg) demonstrated significant neuroprotective activity even after delayed administration at 1 h, 3 h and 5 h after cerebral ischemia and reperfusion. Forsythoside B 20 mg/kg attenuated histopathological damage as demonstrated by smaller brain infarct size and brain edema, decreased cerebral Evans blue extravasation and myeloperoxidase (MPO) activity, inhibited cerebral phosphor-IkappaB-alpha and nuclear transcription factors kappaB (NF-kappaB) expression. Meanwhile, NF-kappaB expression with immunohistochemical ...
Estrogens are neuroprotective factors for brain diseases, including hypertensive encephalopathy. In particular, the hippocampus is highly damaged by high blood pressure, with several hippocampus functions being altered in humans and animal models of hypertension. Working with a genetic model of primary hypertension, the spontaneously hypertensive rat (SHR), we have shown that SHR present decreased dentate gyrus neurogenesis, astrogliosis, low expression of brain derived neurotrophic factor (BDNF), decreased number of neurons in the hilus of the dentate gyrus, increased basal levels of the estrogen-synthesizing enzyme aromatase, and atrophic dendritic arbor with low spine density in the CA1 region compared to normotensive Wistar Kyoto (WKY) ratsl. Changes also occur in the hypothalamus of SHR, with increased expression of the hypertensinogenic peptide arginine vasopressin (AVP) and its V1b receptor. Following chronic estradiol treatment, SHR show decreased blood pressure, enhanced hippocampus ...
In this study, we developed an in vivo method to determine drug effects on oxidation-induced apoptosis in the zebrafish brain caused by treatment with l-hydroxyglutaric acid (LGA). We confirmed that LGA-induced apoptosis was caused by oxidation by examining the presence of an oxidative product, nitrotyrosine. Next, we examined the effects of 14 characterized neuroprotectants on LGA-treated zebrafish, including: d-methione (d-Met), Indole-3-carbinol, deferoxamine (DFO), dihydroxybenzoate (DHB), deprenyl, l-NAME (N(G)-nitro-l-arginine methyl ester), n-acetyl l-cysteine (l-NAC), 2-oxothiazolidine-4-carboxylate (OTC), lipoic acid, minocycline, isatin, cortisone, ascorbic acid and α-tocopherol. Eleven of 14 neuroprotectants and 7 of 7 synthetic anti-oxidants exhibit significant protection in zebrafish. Buthionine sulfoximine (BSO), used as a negative control, exhibited no significant protective effects. In addition, three blood-brain barrier (BBB) impermeable compounds exhibited no significant effects. Our
TY - JOUR. T1 - Vanilloid VR 1 receptor is involved in rimonabant-induced neuroprotection. AU - Pegorini, Simona. AU - Zani, Alessia. AU - Braida, Daniela. AU - Guerini-Rocco, Chiara. AU - Sala, Mariaelvina. PY - 2006/3. Y1 - 2006/3. N2 - Recently, a potential neuroprotective effect of rimonabant, independent of the CB 1 receptor interaction, has been proposed. In the present study, the role of transient receptor potential channel vanilloid subfamily member 1, named VR 1, on neuroprotective effect of rimonabant, on global cerebral ischemia in gerbils, was investigated. Rimonabant (0.05-3 mg kg -1), given i.p. 5 min after recirculation, dose dependently antagonized the ischemia-induced decrease in electroencephalographic (EEG) total spectral power and restored relative frequency band distribution 7 days after ischemia. Rimonabant (0.125-0.5 mg kg -1) fully prevented ischemia-induced hyperlocomotion 1 day after ischemia and memory impairment evaluated in a passive avoidance task, 3 days after ...
TCTs differ from TCPs by possessing a farnesyl (isoprenoid) rather than a saturated phytyl side chain. The unsaturated side chain of TCT allows for more efficient penetration into tissues that have saturated fatty layers such as the brain and liver.25 Micromolar amounts of TCT, not TCP, have been shown to suppress the activity of hydroxy-3-methylglutaryl coenzyme A reductase.26,27 Our finding that cytosolic, but not nuclear, TCT is neuroprotective is in line with our previous observations characterizing that the molecular targets of TCT in the neuron are cytosolic.5,7 Furthermore, the results showing that at subattomole levels TCT, but TCP, are neuroprotective is consistent with our previous reports claiming that at low doses, the neuroprotective property of TCT is not shared by TCP.5 Efforts to elucidate the mechanisms underlying the neuroprotective properties of TCT led to the finding that glutamate-induced rapid c-Src activation is prevented in the presence of nanomolar concentrations of TCT. ...
Several recent studies have demonstrated that TAT and other arginine-rich cell penetrating peptides (CPPs) have intrinsic neuroprotective properties in their own right. Examples, we have demonstrated that in addition to TAT, poly-arginine peptides (R8 to R18; containing 8-18 arginine residues) as well as some other arginine-rich peptides are neuroprotective in vitro (in neurons exposed to glutamic acid excitotoxicity and oxygen glucose deprivation) and in the case of R9 in vivo (after permanent middle cerebral artery occlusion in the rat). Based on several lines of evidence, we propose that this neuroprotection is related to the peptides endocytosis-inducing properties, with peptide charge and arginine residues being critical factors. Specifically, we propose that during peptide endocytosis neuronal cell surface structures such as ion channels and transporters are internalised, thereby reducing calcium influx associated with excitotoxicity and other receptor-mediated neurodamaging signalling ...
The overall aim of the project is pharmacological and neurochemical profiling of a novel class of compounds, positive allosteric modulators (PAM) of Sigma-1 receptor (Sig-1R), in pre-clinical models of spatial and neurodegenerative cognition impairment and investigate possibilities to regulate the interactions of Sigma-1 and NMDA receptors to discover novel treatment means for Alzheimers disease.. This aim will be achieved by the implementation of the following objectives:. ...
In addition to its original application for treating tuberculosis, rifampicin has multiple potential neuroprotective effects in chronic neurodegenerative diseases including Parkinsons disease (PD)...
BACKGROUND & OBJECTIVE: Alzheimers disease (AD) and Parkinsons disease (PD) affect an increasing number of the elderly population worldwide. The existing treatments mainly improve the core symptoms of AD and PD in a temporary manner and cause alarming side effects. Naturally occurring flavonoids are well-documented for neuroprotective and neurorestorative effects against various neurodegenerative diseases. Thus, we analyzed the pharmacokinetics of eight potent natural products flavonoids for the druggability and discussed the neuroprotective and neurorestorative effects and the underlying mechanisms. CONCLUSION: This review provides valuable clues for the development of novel therapeutics against neurodegenerative diseases ...
Ginkgo biloba is a commonly used herb for peripheral vascular disorders and is thought to improve memory. More than 1,000 clinical studies have examined the effects of ginkgo, and its potential mechanisms of action. Research to evaluate the clinical efficacy of ginkgo has predominantly focused on its potential neuroprotective effects in patients with cognitive impairment, but the effects of ginkgo on healthy individuals have also been examined. Previous authors have reviewed this literature. However, methodological limitations of earlier papers, the volume of new research not included in the original reviews, and identification of other potentially important processes previously overlooked, necessitated another comprehensive review. Therefore, the purpose of this study was to perform a meta-analysis examining the existing ginkgo literature, and further evaluate effect of standardized ginkgo extract treatment on psychosocial and cognitive functioning. Results revealed a significant
Glaucoma is a group of chronic progressive optic neuropathies commonly characterized by elevated intraocular pressure (IOP) (a subset of glaucoma patients display neurodegenerative effects at normal IOP) leading to axonal degeneration, optic nerve head cupping and apoptosis of retinal ganglion cell death (RGCs), which result in visual field defects and blindness. While there are medications available to lower IOP, there is an unmet need for neuroprotective treatments for glaucoma, since some neurodegenerative effects persist despite lowering IOP. The main focus of this study was on the class 4 POU domain transcription factor, Brn3b, which has been shown to play a key role in the development of RGCs. Two previous studies from other labs showed that a decrease in Brn3b expression occurs in animal model of glaucoma. A recent publication from our laboratory demonstrated neuroprotective effects of adeno-associated virus (AAV) mediated expression of Brn3b in a rat model of ocular hypertension. This research
This thesis examined the effects of neonatal acute immune activation with the endotoxin, lipopolysaccharide (LPS) on postnatal days 3 and 5 on adolescent anxiety-like behaviour in rats before and after a stress period. Previous research has shown that adults rats exposed to LPS during the neonatal stage show anxiety-like behaviour following a period of stress. This thesis investigated this effect in adolescence. The present results showed significantly higher anxiety-like behaviour in saline controls, and a potential neuroprotective effect of low dose LPS (15 µg/kg) contrary to what was reported in adult rats. As well, a phase of stressful, aversive conditioning (conditioned disgust) did not elicit anxiety-like behaviour in LPS-treated adolescent rats. The findings of this study provide novel findings about the adolescent period, and suggest the use of no injection controls for neonatal research. This thesis presents data that suggests the importance of no injection controls in future neonatal
Our results provide the first direct evidence of a neural basis for bilingual cognitive control advantages in aging. Our bilingual and monolingual groups were matched on relevant demographic and neuropsychological scores that have been linked with cognitive control performance including education level, SES, and IQ. In addition, bilingual participants did not score higher than their monolingual peers on tests of simple working memory span. Nevertheless, across two experiments using different subjects, older adult bilinguals switched between perceptual tasks significantly faster than their monolingual peers. Experiment 2 revealed that older adult bilinguals showed a pattern of fMRI results similar to the younger adult groups: they outperformed monolingual older adults while requiring less activation in several frontal brain regions linked with effortful processing. The details of these findings and their implications concerning the potential neuroprotective effects of bilingualism on cognitive ...
Vascular endothelial growth factor (VEGF) has previously been shown to display neuroprotective effects following ischemia, suggesting that VEGF may potentially be applied as a neuroprotective agent for the treatment of other neurological diseases. In this study, we investigated the neuroprotective capacity of VEGF in a model of Parkinsons disease. VEGF was found to be neuroprotective against cell death of primary E14 murine ventral mesencephalic neurons induced by 6-hydroxydopamine (6-OHDA) treatment in vitro. Further, rats receiving a continuous infusion of VEGF into the striatum via encapsulated hVEGF-secreting cells (baby hamster kidney-VEGF) displayed a significant decrease in amphetamine-induced rotational behavior and a significant preservation of tyrosine hydroxylase-positive neurons and fibers compared with control animals. VEGF likely functions via direct mechanisms by signaling through the neuropilin receptor expressed upon dopaminergic neurons in response to 6-OHDA treatment. ...
TY - JOUR. T1 - GOSPEL. T2 - a neuroprotective protein that binds to GAPDH upon S-nitrosylation.. AU - Sen, Nilkantha. AU - Hara, Makoto R.. AU - Ahmad, Abdullah Shafique. AU - Cascio, Matthew B.. AU - Kamiya, Atsushi. AU - Ehmsen, Jeffrey T.. AU - Aggrawal, Nishant. AU - Hester, Lynda. AU - Doré, Sylvain. AU - Snyder, Solomon H.. AU - Sawa, Akira. N1 - Funding Information: This work was supported by United States Public Health Service grants MH-084018 and MH-069853 (A.S.); DA-00266 (S.H.S.); and Research Scientist Award DA-00074 (S.H.S.); and grants from the Stanley, National Alliance for Research in Schizophrenia and Affective Disorders, Core Huntingtons Disease Initiative, and S-R Foundations (A.S.). We thank Yukiko L. Lema for preparing figures and organizing the manuscript. We appreciate technical assistance by Mr. S. Seshadri, Mr. J. Park, Ms. X. Luo, and Ms. L. Hanle. PY - 2009/7/16. Y1 - 2009/7/16. N2 - We recently reported a cell death cascade whereby cellular stressors activate ...
2) To evaluate the neuroprotective effect of UA, rat neural retinal explants were cultured in low-serum medium and treated with UA at intraocular concentration ranges ( 10, 50 and 500 ng/ml) found in patients. Markers of apoptosis (caspase 3) and Necrosis (LDH, RIP) were analyzed by western immunoblotting. Immunohistochemistry was performed on sections of fixed retinas (cone arrestin, peanut agglutinin). Results : 1) UA was found in vitreous and/or subretinal fluid in 12 patients (57%). The concentrations of UA were higher in patients who were treated 8 hours or more before surgery. Controls patients did not present UA in subretinal fluid samples (p=0.04, vs treated patients). The UA concentration in subretinal fluid was correlated with the total protein concentration (p,0.0001 ...
Yolkin- A Polypeptide Complex Isolated From Chicken Egg Yolk with Potential Neuroprotective and Antioxidative Activity, Agnieszka Zablocka, Aleksandra Zambrowicz, Jozefa Macala, Wi
Current Gerontology and Geriatrics Research is a peer-reviewed, Open Access journal aims at scientists, geriatricians, health professionals interested in molecular, cellular, organismal aspects of gerontological research and in diagnosis, treatment, evaluation and educational aspects of geriatrics research. The journal also highlights new discoveries, approaches as well as technical developments in basic, clinical and discovery driven translational research.
TY - JOUR. T1 - A systematic review of biomarkers for disease progression in Alzheimers disease. AU - McGhee, David J M. AU - Ritchie, Craig W. AU - Thompson, Paul A. AU - Wright, David E. AU - Zajicek, John P. AU - Counsell, Carl E. PY - 2014/2/18. Y1 - 2014/2/18. N2 - BackgroundUsing surrogate biomarkers for disease progression as endpoints in neuroprotective clinical trials may help differentiate symptomatic effects of potential neuroprotective agents from true slowing of the neurodegenerative process. A systematic review was undertaken to determine what biomarkers for disease progression in Alzheimers disease exist and how well they perform.MethodsMEDLINE and Embase (1950-2011) were searched using five search strategies. Abstracts were assessed to identify papers meriting review in full. Studies of participants with probable Alzheimers disease diagnosed by formal criteria were included. We made no restriction on age, disease duration, or drug treatment. We only included studies with a ...
Poulsens previous work on developing therapies to treat injuries to the central nervous system strongly suggest that phenoxybenzamine is highly neuroprotective when given within eight hours after a severe TBI.. Phenoxybenzamine is an FDA-approved treatment for humans and animals to reduce hypertension and excessive sweating associated with adrenal tumors, but Poulsen says it may also may exert a neuroprotective effect by reducing neuroinflammation after TBI. ...
We recently reported that adeno-associated virus serotype 1 (AAV1) transduction of murine nigral dopaminergic (DA) neurons with constitutively active ras homolog enriched in brain with a mutation of serine to histidine at position 16 [Rheb(S16H)] induced the production of neurotrophic factors, resulting in neuroprotective effects on the nigrostriatal DA system in animal models of Parkinsons disease (PD). To further investigate whether AAV1-Rheb(S16H) transduction has neuroprotective potential against neurotoxic inflammation, which is known to be a potential event related to PD pathogenesis, we examined the effects of Rheb(S16H) expression in nigral DA neurons under a neurotoxic inflammatory environment induced by the endogenous microglial activator prothrombin kringle-2 (pKr-2 ...
This process appears as a incredible and progressive event that will not stop till reattachment of RPE and neurosensory retina happened .. Process of degeneration begins from first hours of RD (Retinal Detachment) establishment Neuroprotection of photoreceptor following RD is a novel and debatable discussion encountered in recent years .. How to stop this phenomena and neuroprotective agent role in this issue are a new interest of researcher.. In the study the investigators are planning to perform a clinical trial to demonstrate the minocycline neuroprotective effect in a double blind design as this impact has been implicated previously in a animal study ...
Cerebral infarction is the most common form of stroke (80% of strokes). Stroke is the first cause of acquired disability, and the 2nd cause of dementia and death. The only approved treatment in the first 4.5 hour is intravenous rt-PA thrombolysis (Actilyse ®) whose objective is recanalization of occluded artery and reperfusion of the brain parenchyma. Few patients are treated (1-5%) and they keep disability in 50-60% of cases. This handicap is mainly correlated to the final infarct size. The objective of neuroprotective treatments is to reduce the final size of the cerebral infarction. The per-conditioning remote ischemic (Per-CID) showed a neuroprotective effect in cerebral ischemia by reducing the final size of cerebral infarction animal models. The per-CID corresponds, in cases of cerebral ischemia, to iterative ischemia realization of a member with a cuff. In humans, the per-CID has shown a cardioprotective effect in a randomized control trial involving 250 patients within 6 first hours of ...
Neuroprotective drugs might seem impractical or improbable right now, after two big clinical trials testing progesterone in traumatic brain injury didnt work out. But one close observer of drug discovery is predicting a coming boom in brain medicines. Maybe this research, which Emory scientists have been pursuing for a long time, will be part of it.. In the 1990s, neuroscientists identified a class of drugs that showed promise in the area of stroke. NMDA receptor antagonists could limit damage to the brain in animal models of stroke. But one problem complicated testing the drugs in a clinical setting: the side effects included disorientation and hallucinations.. Now researchers have found a potential path around this obstacle. The results were published in Neuron.. “We have found neuroprotective compounds that can limit damage to the brain during ischemia associated with stroke and other brain injuries, but have minimal side effects,†says senior author Stephen Traynelis, ...
Li, C., Chen, T., Zhou, H., Feng, Y., Hoi, M. P., Ma, D., Zhao, C., et al. (2018). BHDPC Is a Novel Neuroprotectant That Provides Anti-neuroinflammatory and Neuroprotective Effects by Inactivating NF-κB and Activating PKA/CREB.. Frontiers in pharmacology, 9 614. https://doi.org/10.3389/fphar.2018.00614 ...
Klotho is a transmembrane protein with a wide spectrum of activity. The human Klotho gene shows 86% amino acid identity with the mouse protein. Many important pleiotropic functions of the Klotho protein have been revealed. Amongst them, there is a regulation of nitric oxide production, suppression of oxidative stress and inflammation, influence on the insulin-like growth factors and fibroblast growth factors signaling, modulation of calcium and phosphate metabolism, synthesis of vitamin D and other. Two forms of the Klotho protein are known. The secreted form strongly inhibits the oxidative stress, and, in humans, is more dominant than the membrane form. Studies on a mouse model resulted in the finding of the anti-aging effect of the Klotho protein. This activity is mainly associated with the suppression of oxidative stress, as well as it could be related to neuroprotective, cardioprotective, and metabolic functions.It might be speculated that Klotho, regarded as a neuroprotective factor, may ...
Bioactivation of 3-n-butylphthalide via sulfation of its major metabolite 3-hydroxy-NBP: mediated mainly by sulfotransferase 1A1. - Xingxing Diao, Xiaoyan Pang, Cen Xie, Zitao Guo, Dafang Zhong, Xiaoyan Chen
This review highlights our investigations into the neuroprotective efficacy of estradiol and other estrogenic agents in a clinically relevant animal model of transient global ischemia, which causes selective, delayed death of hippocampal CA1 neurons and associated cognitive deficits. We find that es …
The diagnosis of Parkinsons disease relies on expert opinion. Autopsy studies, however, have demonstrated that even experienced neurologists misdiagnose Parkinsons disease in about a quarter out of a hundred cases. Diagnostic accuracy at disease onset, when neuroprotective treatment is anticipated to be most effective, is even lower. Thus, there is a crucial need for biomarkers that are disease-specific and which precisely identify early disease stages.Traditional studies of blood from Parkinsons disease patients have analyzed expression levels of one gene or gene product at a time. We plan to take advantage of gene chip technology allowing expression analysis of up to 22,000 genes on a single glass slide, known as microarray. We hypothesize that a comparison of the gene chip analyses of blood samples from Parkinsons disease patients and normal controls or patients with other neurological diseases will identify a set of signature genes with characteristic expression in patients with Parkinsons
BioAssay record AID 780551 submitted by ChEMBL: Neuroprotective activity against Sprague-Dawley rat embryo cortex NSC assessed as reduction of mRNA ratio of bcl2 to bax at 10 uM after 2 days by RT-PCR method relative to DMSO-treated control.
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Orexin-A is a neuropeptide with potent neuroprotective activity towards cerebral ischemia-reperfusion (I/R) injury, but few studies have attempted to elucidate the mechanism. Herein, we performed global gene expression profiling of the hippocampus following reperfusion with Orexin-A using RNA sequencing (RNA-seq). RNA-seq identified 649 differentially expressed genes (DEGs) in the Orexin-A group compared with saline controls (I/R group), of which 149 were up-regulated and 500 were down-regulated. DEGs were confirmed using qRT-PCR, their molecular functions, biological processes and molecular components were explored using Gene Ontology (GO) analysis and 206 KEGG pathways were associated with Orexin-A treatment ...
Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning. A protective enzyme against harmful proteins that is up-regulated by breathing slower. By increasing CO2 levels. By creating an anoxic environment.. ...
Huntingtons disease (HD) is characterized by progressive brain neurodegeneration, often leading to dementia. A mutation in the huntingtin protein and nuclear accumulation of the mutant are associated with the pathology of HD, but it is not yet clear how the mutant protein induces the death of neurons. Growth factors that promote cell survival are attractive therapeutic agents for HD; Humbert et al. report that insulin-like growth factor 1 (IGF-1) shows just such neuroprotective potential. IGF-1 promotes cell survival through activation of the serine-threonine kinase Akt. The study shows that a specific serine residue in huntingtin is phosphorylated by Akt both in vitro and in neuronal cells in response to IGF-1. Furthermore, this IGF-1-induced modification blocked the formation of nuclear inclusions and neuronal apoptosis. Brain samples from HD patients also showed decreased amounts of Akt. Phosphorylation by Akt may alter HD interactions with proteins that promote apoptosis and, hence, ...
Antioxidant and neuroprotective effects induced by cannabidiol and cannabigerol in rat CTX-TNA2 astrocytes and isolated cortexes.
Neuroprotective effect of green tea extract in experimental ischemia-reperfusion brain injury Author: Jin Tae Hong and Seung Rel Ryu and Hye Jin Kim and Jong Kwon Lee and Sun Hee Lee and Dai Byung Kim and Yeo Pyo Yun and Jong Hoon Ryu and Byung Mu Lee and Pu Young Kim Eicosanoids accumulation and formation of oxygen fr
The exceptional results of the studies demonstrate that the bioproduct significantly increases the levels of dopamine and norepinephrine in the body and at the same time improves the symptoms of the disease. The report shows that no undesirable side effects have been noticed during the clinical trial. The studies also reveal a robust neuroprotective potential that could help in the field of prevention and enhance slowing down the disease progression. Is this a significant step forward in the fight against Parkinsons disease?. Origins of Parkinsons disease. Parkinsons disease has its roots in the progressive degeneration of dopaminergic neurons. The primary symptoms are well known: stiffness, tremors, slow movements, and depression. In addition, there is a multitude of other symptoms that make this disease extraordinarily debilitating and painful to live on a daily basis. It is physically, psychologically and socially exhausting for patients as well as for the families and ...
Author: Moosmann, B. et al.; Genre: Journal Article; Published in Print: 1999; Title: The antioxidant neuroprotective effects of estrogens and phenolic compounds are independent from their estrogenic properties.
Danysz W.; Parsons C.G.; Karcz-Kubicha M.; Hesselink M.; Wenk G.L.; Lazarewicz J.; Popik P.; Gold M.; Kalvinsh I.; Piskunova I.; Rozhkov E. Novel systemically-active antagonists of the glycine site of NMDA receptor - neuroprotective effects and behavioural characterisation . Abstracts, International Conference Trends in neuroprotective drugs: Design, pharmacology and clinics = TNPD; May 29-June 1; Riga, Latvia, Eds.; Pharmacol. Toxicol.: Vol.80, Supp.1, 1997; 17 ...
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Botanys whole-plant organic supplements include beneficial natural extracts, phytochemicals, flavonoids, sterols, antioxidants and neuroprotectants.
Brain, Transient, Gelatinase, Ischemia, Mice, Concentration, Brain Ischemia, Cerebral Ischemia, Gelatin, Inhibition, Growth, Hippocampus, Neuroprotective Effects, Tea, Tunel, Oxygen, Artery, Brain Infarction, Infarction, Neuroprotective Effect